Yuvashree Muralidaran and Pragasam Viswanathan
Diabetic cardiomyopathy
(DCM), one among the macrovascular complications of diabetes is the leading cause of mortality around the globe. The emergence of DCM irrespective of other cardiovascular diseases (CVD) necessitates a deeper insight into its occurrence and mechanism of development. This review summarizes the different stages in DCM progression based on molecular, cellular and functional level. The early stage in DCM involves
oxidative stress
and endoplasmic reticulum stress concomitant with O-linked glycosylation of receptors, and extracellular matrix (ECM) proteins, and formation of advanced glycation end products (AGE). This further influences myocyte apoptosis and steatosis, which is followed by fibrosis and remodeling, thus altering the physiological functioning of heart. It has been postulated that, microbuminuria (MA) which is an indicator of renal failure is also an early predictor of DCM. Currently, focus on epigenetic modifications, as observed in diabetics with renal failure is of critical importance to unveil the mystery behind the association of DCM and MA. Albeit, we examine DCM in a mechanistic approach, the major reason that remains unnoticed is glycemic excursion (GE). ACCORD, DCCT and EDIC studies have reported that the persistent effect in CVD is due to transient
hyperglycemia
. Hence it is predicted that, treatment strategies focusing on genetic level, along with maintaining persistent blood glucose would be more effectual. Besides, designing treatment regimen for patients with renal failure would be a preventive strategy for diabetic cardiomyopathy when their state towards DCM incidence is also considered and monitored precisely.
